We proposed that the higher incidence of sleep fragmentation, sympathovagal imbalance and baroreceptor reflex impairment during quiet sleep may play a critical role in late-sleep-related cardiovascular events. Polysomnographic recording was performed through wireless transmission using freely moving Wistar–Kyoto rats over 24 h. The low-frequency power of arterial pressure variability was quantified to provide an index of vascular sympathetic activity. Spontaneous baroreflex sensitivity was assessed by slope of arterial pressure–RR linear regression. As compared with early-light period (Zeitgeber time 0–6 h), rats during the late-light period (Zeitgeber time 6–12 h) showed lower accumulated quiet sleep time and higher paradoxical sleep time; furthermore, during quiet sleep, the rats showed a lower δ% of electroencephalogram, more incidents of interruptions, higher σ% and higher β% of electroencephalogram, raised low-frequency power of arterial pressure variability value and lower baroreflex sensitivity parameters. During the light period, low-frequency power of arterial pressure variability during quiet sleep had a negative correlation with accumulated quiet sleep time and δ% of electroencephalogram, while it also had a positive correlation with σ% and β% of electroencephalogram and interruption events. However, late-sleep-related raised sympathetic activity and sleep fragmentation diminished when an α1-adrenoceptor antagonist was given to the rats. Our results suggest that the higher incidence of sleep fragmentation and sympathovagal imbalance during quiet sleep may play a critical role in late-sleep-related cardiovascular events. Such sleep fragmentation is coincident with an impairment of baroreflex sensitivity, and is mediated via α1-adernoceptors.